| First Author | Qian X | Year | 2017 |
| Journal | J Cell Mol Med | Volume | 21 |
| Issue | 7 | Pages | 1431-1444 |
| PubMed ID | 28224733 | Mgi Jnum | J:345281 |
| Mgi Id | MGI:6838140 | Doi | 10.1111/jcmm.13072 |
| Citation | Qian X, et al. (2017) NK1.1(-) CD4(+) NKG2D(+) T cells suppress DSS-induced colitis in mice through production of TGF-beta. J Cell Mol Med 21(7):1431-1444 |
| abstractText | CD4(+) NKG2D(+) T cells are associated with tumour, infection and autoimmune diseases. Some CD4(+) NKG2D(+) T cells secrete IFN-gamma and TNF-alpha to promote inflammation, but others produce TGF-beta and FasL to facilitate tumour evasion. Here, murine CD4(+) NKG2D(+) T cells were further classified into NK1.1(-) CD4(+) NKG2D(+) and NK1.1(+) CD4(+) NKG2D(+) subpopulations. The frequency of NK1.1(-) CD4(+) NKG2D(+) cells decreased in inflamed colons, whereas more NK1.1(+) CD4(+) NKG2D(+) cells infiltrated into colons of mice with DSS-induced colitis. NK1.1(-) CD4(+) NKG2D(+) cells expressed TGF-beta and FasL without secreting IFN-gamma, IL-21 and IL-17 and displayed no cytotoxicity. The adoptive transfer of NK1.1(-) CD4(+) NKG2D(+) cells suppressed DSS-induced colitis largely dependent on TGF-beta. NK1.1(-) CD4(+) NKG2D(+) cells did not expressed Foxp3, CD223 (LAG-3) and GITR. The subpopulation was distinct from NK1.1(+) CD4(+) NKG2D(+) cells in terms of surface markers and RNA transcription. NK1.1(-) CD4(+) NKG2D(+) cells also differed from Th2 or Th17 cells because the former did not express GATA-3 and ROR-gammat. Thus, NK1.1(-) CD4(+) NKG2D(+) cells exhibited immune regulatory functions, and this T cell subset could be developed to suppress inflammation in clinics. |
